The proposed research plan is a direct test of the hypothesis that the initiation and maintenance of growth control is a function of intercellular adhesion which in turn is probably affected by macromolecular events at the level of the cell membrane. These phenomena must involve the interaction of specific molecules that trigger further changes on the surfaces of the participating cells during the adhesion and recognition processes. Since transformed cells have a decreased level of tissue organization, altered growth and adhesive properties, these differences should be reflected in an altered membrane architecture and/or molecular fine structure. Transformed and normal cells show such differences with respect to complex carbohydrates and lipids. In some instances complex carbohydrates have been implicated to play a role in growth regulation and intercellular adhesion and/or recognition which ultimately governs morphogenesis and metastasis of tumor cells. We have demonstrated that a steroid and a glycolipid, both synthesized by SV 40 transformed 3T3 cells but not by normal 3T3 cells, inhibit the intercellular adhesive process for 3T3 cells. In addition, we have obtained data that suggest the involvement of glycoproteins in cell cycle specific intercellular adhesion. This phenomenon is only observed with parent CHO-K1 cells and not with ricin resistant clones. Our main objectives are: (1) to evaluate the structure and biosynthesis of the steroid component, (2) to elucidate the structure of the glycolipid, (3) to determine the mechanism by which those two lipid components interact with the adhesive process, and (4) to study normal and lectin resistant clones with respect to the biochemistry of cell cycle specific adhesion.